Fig. 5: rpoB substitutions upregulate the prdR locus.

a, PCA denoting segregation of the total lipid classes obtained for the WT and RpoB mutants. b, The 25 significantly differentially expressed loci identified in both RNA-seq and proteomics. The fold change value for RNA-seq is shown in the colour scale (log₂-transformed fold change). S+T, the double RpoB(S491F)/RpoC(T634K) mutant. c, Daptomycin susceptibility testing results for the WT and rpoB backgrounds (S491F, G482D or H486Y) with prdR, prdA or prdB deleted (n = 3). The MIC for each strain is shown without error bars as no variation between independent biological replicates was observed. d, PCA denoting the segregation of the total lipid classes obtained for the WT, S491F mutant, WT^EV and WT^prdR. e, The zeta potential (measured in mV). The points represent each biological replicate (n = 3), and the lines represent the median and interquartile range. Data were analysed using one-way analysis of variance (ANOVA) with correction for multiple testing using the Dunnett method, comparing WT versus RpoB mutant and WT^EV versus WT^prdR. f, Binding of BoDIPY–DAP, represented as relative fluorescence units (RFU). The points represent each biological replicate (n = 5) and the lines represent the median and interquartile range. Data were analysed using one-way ANOVA with correction for multiple testing using the Dunnett method, comparing WT versus RpoB mutant and WT^EV versus WT^prdR. Exact P values are provided when the P value is above P < 0.0001.

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